Curr Opin Investig Drugs 2002 Jun;3(6):859-64
Smith PF.
Department of Pharmacology and Toxicology, School of Medical Sciences,
University of Otago, Dunedin, New Zealand.

There is a large amount of evidence to support the view that the psychoactive
ingredient in cannabis, delta9-tetrahydrocannabinol (delta9-THC), and cannabinoids
in general, can reduce muscle spasticity and pain under some circumstances.

Cannabinoid (CB1) receptors in the CNS appear to mediate both of these
effects and endogenous cannabinoids may fulfil these functions to some
extent under normal circumstances.

However, in the context of multiple
sclerosis (MS), it is still questionable whether cannabinoids are superior
to existing, conventional medicationsfor the treatment of spasticity and
pain.

In the case of spasticity, there are too few controlled clinical
trials to draw any reliable conclusion at this stage.

In the case of pain,
most of the available trials suggest that cannabinoids are not superior
to existing treatments; however, few trials have examined chronic pain
syndromes that are relevant to MS.

Whether or not cannabinoids do have
therapeutic potential in the treatment of MS, a further issue will be whether
synthetic cannabinoids should be used in preference to cannabis itself.

Smoking cannabis is associated with significant risks of lung cancer and
other respiratory dysfunction.

Furthermore, delta9-THC, as a broad-spectrum
cannabinoid receptor agonist, will activate both CB1 and CB2 receptors.

Synthetic cannabinoids, which target specific cannabinoid receptor subtypes
in specific parts of the CNS, are likely to be of more therapeutic use
than delta9-THC itself.

If rapid absorption is necessary, such synthetic
drugs could be delivered via aerosol formulations.